Oxidative Stress, Mitochondrial Dysfunction, and Aβ Pathology: Converging Pathways in Aging and Neurodegeneration

Dear Colleagues,

This Special Issue highlights cutting-edge research in oxidative stress and mitochondrial biology, with a particular focus on their roles in aging, regulated cell death, and neurodegenerative conditions, including amyloid-β (Aβ) pathology.

Oxidative stress arises from imbalanced levels of reactive oxygen and nitrogen species (RONS), which serve as key modulators of physiological processes such as host defense, apoptosis, and cellular senescence. Both endogenous and exogenous sources contribute to reactive and non-reactive oxidative stress.

Mitochondria are central to RONS generation, functioning within the electron transport chain (ETC) to drive ATP production via oxidative phosphorylation (OXPHOS). While RONS are essential signaling molecules, their dysregulation leads to inflammatory damage, apoptosis, and tissue degeneration. These disruptions accelerate aging, contribute to Aβ accumulation and aggregation, and promote the progression of neurodegenerative diseases including Alzheimer's disease.

Recent studies have advanced our understanding of oxidative stress regulation, mitochondrial dynamics, and Aβ-associated pathology, paving the way for novel therapeutic strategies and standardized management protocols. This Special Issue welcomes original research and review articles that explore oxidative stress mitigation, mitochondrial function, and molecular mechanisms in the context of aging, neurodegeneration, and regulated cell death pathways.

Dr. Swapnil Pandey
Dr. Laxmi Rathor
Dr. Ashish Shukla
Guest Editors

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